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Diallyl trisulfide-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by reactive oxygen species-dependent destruction and hyperphosphorylation of Cdc 25 C.
Oncogene. 2005 Sep 15; 24(41):6256-68.O

Abstract

Molecular mechanism of cell cycle arrest caused by diallyl trisulfide (DATS), a garlic-derived cancer chemopreventive agent, has been investigated using PC-3 and DU 145 human prostate cancer cells as a model. Treatment of PC-3 and DU 145 cells, but not a normal prostate epithelial cell line (PrEC), with growth suppressive concentrations of DATS caused enrichment of the G(2)-M fraction. The DATS-induced cell cycle arrest in PC-3 cells was associated with increased Tyr(15) phosphorylation of cyclin-dependent kinase 1 (Cdk 1) and inhibition of Cdk 1/cyclinB 1 kinase activity. The DATS-treated PC-3 and DU 145 cells also exhibited a decrease in the protein level of Cdc 25 C and an increase in its Ser(216) phosphorylation. The DATS-mediated decrease in protein level and Ser(216) phosphorylation of Cdc 25 C as well as G(2)-M phase cell cycle arrest were significantly attenuated in the presence of N-acetylcysteine implicating reactive oxygen species (ROS) in cell cycle arrest caused by DATS. ROS generation was observed in DATS-treated PC-3 and DU 145 cells. DATS treatment also caused an increase in the protein level of Cdk inhibitor p21, but DATS-induced G(2)-M phase arrest was not affected by antisense-mediated suppression of p21 protein level. In conclusion, the results of the present study indicate that DATS-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by ROS-mediated destruction and hyperphosphorylation of Cdc 25 C.

Authors+Show Affiliations

Department of Pharmacology and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15940258

Citation

Xiao, Dong, et al. "Diallyl Trisulfide-induced G(2)-M Phase Cell Cycle Arrest in Human Prostate Cancer Cells Is Caused By Reactive Oxygen Species-dependent Destruction and Hyperphosphorylation of Cdc 25 C." Oncogene, vol. 24, no. 41, 2005, pp. 6256-68.
Xiao D, Herman-Antosiewicz A, Antosiewicz J, et al. Diallyl trisulfide-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by reactive oxygen species-dependent destruction and hyperphosphorylation of Cdc 25 C. Oncogene. 2005;24(41):6256-68.
Xiao, D., Herman-Antosiewicz, A., Antosiewicz, J., Xiao, H., Brisson, M., Lazo, J. S., & Singh, S. V. (2005). Diallyl trisulfide-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by reactive oxygen species-dependent destruction and hyperphosphorylation of Cdc 25 C. Oncogene, 24(41), 6256-68.
Xiao D, et al. Diallyl Trisulfide-induced G(2)-M Phase Cell Cycle Arrest in Human Prostate Cancer Cells Is Caused By Reactive Oxygen Species-dependent Destruction and Hyperphosphorylation of Cdc 25 C. Oncogene. 2005 Sep 15;24(41):6256-68. PubMed PMID: 15940258.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diallyl trisulfide-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by reactive oxygen species-dependent destruction and hyperphosphorylation of Cdc 25 C. AU - Xiao,Dong, AU - Herman-Antosiewicz,Anna, AU - Antosiewicz,Jedrzej, AU - Xiao,Hui, AU - Brisson,Marni, AU - Lazo,John S, AU - Singh,Shivendra V, PY - 2005/6/9/pubmed PY - 2005/12/13/medline PY - 2005/6/9/entrez SP - 6256 EP - 68 JF - Oncogene JO - Oncogene VL - 24 IS - 41 N2 - Molecular mechanism of cell cycle arrest caused by diallyl trisulfide (DATS), a garlic-derived cancer chemopreventive agent, has been investigated using PC-3 and DU 145 human prostate cancer cells as a model. Treatment of PC-3 and DU 145 cells, but not a normal prostate epithelial cell line (PrEC), with growth suppressive concentrations of DATS caused enrichment of the G(2)-M fraction. The DATS-induced cell cycle arrest in PC-3 cells was associated with increased Tyr(15) phosphorylation of cyclin-dependent kinase 1 (Cdk 1) and inhibition of Cdk 1/cyclinB 1 kinase activity. The DATS-treated PC-3 and DU 145 cells also exhibited a decrease in the protein level of Cdc 25 C and an increase in its Ser(216) phosphorylation. The DATS-mediated decrease in protein level and Ser(216) phosphorylation of Cdc 25 C as well as G(2)-M phase cell cycle arrest were significantly attenuated in the presence of N-acetylcysteine implicating reactive oxygen species (ROS) in cell cycle arrest caused by DATS. ROS generation was observed in DATS-treated PC-3 and DU 145 cells. DATS treatment also caused an increase in the protein level of Cdk inhibitor p21, but DATS-induced G(2)-M phase arrest was not affected by antisense-mediated suppression of p21 protein level. In conclusion, the results of the present study indicate that DATS-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by ROS-mediated destruction and hyperphosphorylation of Cdc 25 C. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/15940258/Diallyl_trisulfide_induced_G_2__M_phase_cell_cycle_arrest_in_human_prostate_cancer_cells_is_caused_by_reactive_oxygen_species_dependent_destruction_and_hyperphosphorylation_of_Cdc_25_C_ L2 - http://dx.doi.org/10.1038/sj.onc.1208759 DB - PRIME DP - Unbound Medicine ER -